The dose of simulated solar ultraviolet light on human skin (SSUV; UVA and UVB) is lower than the dose (0.75 minimum erythema dose, MED) that causes mild redness and swelling of the skin on the first day after exposure, and can directly detect human stratum corneum alpha-fertility Phenol is reduced by nearly 50%, and alpha-tocopherol in mouse stratum corneum is reduced by 85%.
Therefore, the consumption of alpha-tocopherol in the stratum corneum is considered to be a very early and sensitive result of photooxidative damage to the skin. The high sensitivity of vitamin E in the stratum corneum to SSUV may be due to the lack of a common antioxidant system in the stratum corneum. Ascorbate is a major hydrophilic co-antioxidant that can recycle photo-oxidized α-tocopherol. Compared with the content in epidermis and dermal tissue, the content is only in the stratum corneum of mice and humans at a very low level. .
There are two ways to consume vitamin E: a) Direct absorption of ultraviolet UVB radiation. b) Indirectly by consuming excited state singlet oxygen or active oxygen intermediate products, these intermediate products are produced when the photosensitizer absorbs ultraviolet light, which are also in the ultraviolet range. Since both UVB and UVA have been shown to consume α-tocopherol in mice, these two mechanisms may be related.
The maximum absorption peaks of α-tocopherol and γ-tocopherol are between 290-295 nm, which exactly corresponds to the ultraviolet band in the solar spectrum. Interestingly, most of the UVB in the 290-300 nm band on the earth is also absorbed by the human stratum corneum. In addition, in the hairless mouse skin homogenate, when α-tocopherol is at the position of the maximum absorption wavelength in UVR, the consumption of α-tocopherol is also the largest.
This consistency indicates that α-tocopherol will be directly destroyed in the process of absorbing short-wavelength UVB.
In fact, when UVB irradiates the skin, free radicals are formed. The direct consumption of alpha-tocopherol and the formation of free radicals may also affect other endogenous antioxidant pools. As mentioned earlier, α-tocopherol can easily be converted from a free radical state to α-tocopherol under the action of ascorbate and other reducing agents, and these reducing agents can be reduced again by glutathione.
In addition to being directly consumed by UVB, α-tocopherol can also be consumed as an antioxidant activity blocker. Intrinsic photosensitizers (such as porphyrins, riboflavins, quinones and bilirubins) can absorb UVB and UVA photons, causing their electrons to be in an excited state. The excited state sensitizer can then react with another substrate (type I reaction) to form free radicals or radical ions, or react with oxygen (type II reaction) to form singlet oxygen. Photosensitizers, such as melanin, are present in different amounts in the stratum corneum. Therefore, their potential to generate or inhibit free radicals is related to the wavelength of UV absorption, which may regulate the consumption of alpha-tocopherol during/after sun exposure. Another exogenous source of irritation that affects skin vitamin E levels is air pollutants-the effect of ozone on skin antioxidants: no vitamin E consumption was observed when analyzing full-thickness skin. When the skin layer was analyzed separately, When detecting the depletion of α-tocopherol in the outer layer of the epidermis, it was found that ozone itself was too active to penetrate into the skin, and directly reacted quickly with skin barrier lipids and proteins. Therefore, it can be proved that the stratum corneum is the skin layer most sensitive to ozone-induced vitamin E depletion. In addition, it has been demonstrated that vitamin E in the stratum corneum is highly sensitive to topical benzoyl peroxide.